Changes in the Profiles of Chemokines Secreted by Endothelial Cells and Monocytes under Different Coculturing Conditions

Starickova, E. A.; Sokolov, D. N.; Selkov, S. A.; Freidlin, I. S.

doi:10.1007/s10517-011-1165-7

Cited by 4 publications

(2 citation statements)

References 7 publications

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“…This model is suggested by long-lasting elevation in cytokines even after the period of acute illness has passed. It is notable that both CCL2 and CXCL10, which are increased 50 days after CLP, have been shown in vitro to be induced by TNFα in immune and endothelial cells [ 73 , 74 ] and that TNFα also induces neuronal expression of these cytokines [ 75 ]. Conversely, CCR2 mediated signaling may potentiate release of TNFα from macrophages [ 76 ] and also contributes to dysfunction of the blood brain barrier [ 77 ].…”

Section: Discussionmentioning

confidence: 99%

Cecal Ligation and Puncture Results in Long-Term Central Nervous System Myeloid Inflammation

et al. 2016

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Survivors of sepsis often experience long-term cognitive and functional decline. Previous studies utilizing lipopolysaccharide injection and cecal ligation and puncture in rodent models of sepsis have demonstrated changes in depressive-like behavior and learning and memory after sepsis, as well as evidence of myeloid inflammation and cytokine expression in the brain, but the long-term course of neuroinflammation after sepsis remains unclear. Here, we utilize cecal ligation and puncture with greater than 80% survival as a model of sepsis. We found that sepsis survivor mice demonstrate deficits in extinction of conditioned fear, but no acquisition of fear conditioning, nearly two months after sepsis. These cognitive changes occur in the absence of neuronal loss or changes in synaptic density in the hippocampus. Sepsis also resulted in infiltration of monocytes and neutrophils into the CNS at least two weeks after sepsis in a CCR2 independent manner. Cellular inflammation is accompanied by long-term expression of pro-inflammatory cytokine and chemokine genes, including TNFα and CCR2 ligands, in whole brain homogenates. Gene expression analysis of microglia revealed that while microglia do express anti-microbial genes and damage-associated molecular pattern molecules of the S100A family of genes at least 2 weeks after sepsis, they do not express the cytokines observed in whole brain homogenates. Our results indicate that in a naturalistic model of infection, sepsis results in long-term neuroinflammation, and that this sustained inflammation is likely due to interactions among multiple cell types, including resident microglia and peripherally derived myeloid cells.

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Section: Discussionmentioning

confidence: 99%

Cecal Ligation and Puncture Results in Long-Term Central Nervous System Myeloid Inflammation

et al. 2016

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“…15,16 The interaction of CCL5/RANTES with CCR5 plays a pivotal role in the development and progression of atherosclerotic inflammatory disease and influences the evolution of HIV infection. RANTES expression has been detected on atherosclerotic plaques, myofibroblasts, and endothelial cells 17,18 and is mostly upregulated in late stages of atherosclerosis in both murine 19 and human plaques. 17 Moreover, CCL5/RANTES is released by stimulated degranulating platelets so that it can trigger accumulation of shear-resistant monocyte on atherosclerotic, inflamed endothelium.…”

Section: Clinical Perspective On P 2124mentioning

confidence: 99%

Efficacy of the CCR5 Antagonist Maraviroc in Reducing Early, Ritonavir-Induced Atherogenesis and Advanced Plaque Progression in Mice

et al. 2013

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Background-CCR5 plays an important role in atherosclerosis and ischemic cardiovascular diseases, as well as in HIV replication and diffusion. HIV infection is characterized by a high burden of cardiovascular diseases, particularly in subjects exposed to ritonavir-boosted protease inhibitors. Maraviroc, a CCR5 antagonist antiretroviral drug, might provide benefit for patients with M-tropic HIV infections at high risk for cardiovascular diseases. Methods and Results-Exposure to maraviroc limits the evolution and associated systemic inflammation of ritonavirinduced atherosclerotic in ApoE −/− mice and inhibits plaques development in a late model of atherosclerosis in which dyslipidemia plays the main pathogenic role. In ritonavir-treated mice, maraviroc reduced plaque areas and macrophage infiltration; downregulated the local expression of vascular cell adhesion molecule-1, intercellular adhesion molecule-1, monocyte chemoattractant protein-1, and interleukin-17A; and reduced tumor necrosis factor-α and RANTES (regulated on activation, normal T cell expressed, and secreted). Moreover, maraviroc counterregulated ritonavir-induced lipoatrophy and interlelukin-6 gene expression in epididymal fat, along with the splenic proinflammatory profile and expression of CD36 on blood monocytes. In the late model, maraviroc inhibited atherosclerotic progression by reducing macrophage infiltration and lowering the expression of adhesion molecules and RANTES inside the plaques. However, limited systemic inflammation was observed. Conclusions-In a mouse model of genetic dyslipidemia, maraviroc reduced the atherosclerotic progression by interfering with inflammatory cell recruitment into plaques. Moreover, in mice characterized by a general ritonavir-induced inflammation, maraviroc reversed the proinflammatory profile. Therefore, maraviroc could benefit HIV-positive patients with residual chronic inflammation who are at a high risk of acute coronary disease despite a suppressive antiretroviral therapy. To determine these benefits, large clinical studies are needed.

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Effect of THP-1 Cells on the Formation of Vascular Tubes by Endothelial EA.hy926 Cells in the Presence of Placenta Secretory Products

et al. 2017

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We studied the effect of THP-1 cells on the formation of vessel-like structures by endothelial cells in the presence of placenta-conditioned media. Addition of THP-1 cells to endothelial cells cultured in the presence of media conditioned by first-trimester placentas led to an increase in the length of cell tubes and reduced their number in comparison with endothelial cell monoculture. In the presence of media conditioned by third-trimester placentas, THP-1 cells did not affect the length and number of cell tubes formed by endothelial cells. When evaluating the formation of vessel-like structures by endothelial cells in co-culture, marked decrease in the length of cell tubes in the presence of media conditioned by first-trimester placentas vs. third-trimester placentas was noted. No differences in the length and number of cell tubes formed by endothelial cells co-cultured with THP-1 cells in the presence of placental factors from women with preeclampsia and uncomplicated pregnancy were found. These findings can reflect the peculiarities of the influence of macrophages on the formation of blood vessels by endothelial cells in the placenta.

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Changes in the Profiles of Chemokines Secreted by Endothelial Cells and Monocytes under Different Coculturing Conditions

Cited by 4 publications

References 7 publications

Cecal Ligation and Puncture Results in Long-Term Central Nervous System Myeloid Inflammation

Cecal Ligation and Puncture Results in Long-Term Central Nervous System Myeloid Inflammation

Efficacy of the CCR5 Antagonist Maraviroc in Reducing Early, Ritonavir-Induced Atherogenesis and Advanced Plaque Progression in Mice

Effect of THP-1 Cells on the Formation of Vascular Tubes by Endothelial EA.hy926 Cells in the Presence of Placenta Secretory Products

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